Chen Minjie, Li Yanjun, Zhang Li, Wang Jianying, Zheng Chunli, Zhang Xuefeng
School of Mathematics, Physics and Biological Engineering, Inner Mongolia University of Science and Technology, Baotou, 014010, People's Republic of China,
Curr Microbiol. 2015 Feb;70(2):290-7. doi: 10.1007/s00284-014-0710-9. Epub 2014 Oct 25.
Acidithiobacillus ferrooxidans plays a critical role in metal solubilization in the biomining industry, and occupies an ecological niche characterized by high acidity and high concentrations of toxic heavy metal ions. In order to investigate the possible metal resistance mechanism, the cellular distribution of cadmium was tested. The result indicated that Cd(2+) entered the cells upon initial exposure resulting in increased intracellular concentrations, followed by its excretion from the cells during subsequent growth and adaptation. Sequence homology analyses were used to identify 10 genes predicted to participate in heavy metal homeostasis, and the expression of these genes was investigated in cells cultured in the presence of increasing concentrations of toxic divalent cadmium (Cd(2+)). The results suggested that one gene (cmtR A.f ) encoded a putative Cd(2+)/Pb(2+)-responsive transcriptional regulator; four genes (czcA1 A.f , czcA2 A.f , czcB1 A.f ; and czcC1 A.f ) encoded heavy metal efflux proteins for Cd(2+); two genes (cadA1 A.f and cadB1 A.f ) encoded putative cation channel proteins related to the transport of Cd(2+). No significant enhancement of gene expression was observed at low concentrations of Cd(2+) (5 mM) and most of the putative metal resistance genes were up-regulated except cmtR A.f , cadB3 A.f ; and czcB1 A.f at higher concentrations (15 and 30 mM) according to real-time polymerase chain reaction. A model was developed for the mechanism of resistance to cadmium ions based on homology analyses of the predicted genes, the transcription of putative Cd(2+) resistance genes, and previous work.
嗜酸氧化亚铁硫杆菌在生物采矿行业的金属溶解过程中起着关键作用，并且占据着一个以高酸度和高浓度有毒重金属离子为特征的生态位。为了研究可能的金属抗性机制，对镉的细胞分布进行了测试。结果表明，Cd(2+)在初次暴露时进入细胞，导致细胞内浓度增加，随后在后续生长和适应过程中从细胞中排出。通过序列同源性分析来鉴定10个预测参与重金属稳态的基因，并在培养于毒性二价镉（Cd(2+)）浓度不断增加的环境中的细胞中研究这些基因的表达。结果表明，一个基因（cmtR A.f）编码一种假定的Cd(2+)/Pb(2+)响应转录调节因子；四个基因（czcA1 A.f、czcA2 A.f、czcB1 A.f和czcC1 A.f）编码Cd(2+)的重金属外排蛋白；两个基因（cadA1 A.f和cadB1 A.f）编码与Cd(2+)转运相关的假定阳离子通道蛋白。根据实时聚合酶链反应，在低浓度Cd(2+)（5 mM）时未观察到基因表达的显著增强，并且除cmtR A.f、cadB3 A.f和czcB1 A.f外，大多数假定的金属抗性基因在较高浓度（15和30 mM）时上调。基于预测基因的同源性分析、假定的Cd(2+)抗性基因的转录以及先前的研究工作，建立了一个镉离子抗性机制模型。
